Evolving

E l e c t ro c a rd i o g r a p h i c
I n dications for Em er g ent
Reperfusion
Michael J. Lipinski, MD, PhDa, Amal Mattu, MDb,
William J. Brady, MDc,*

KEYWORDS
 ECG  ACS  STEMI  Coronary

KEY POINTS
 Specific high-risk electrocardiogram (ECG) patterns may represent acute myocardial infarction
(AMI) or identify impending AMI that will benefit from early diagnostic coronary angiography.
 The ECG continues to play a critical role in determining which patients require urgent coronary angi-
ography and revascularization.
 It is important to be familiar with obvious indications for emergent cardiac catheterization, and ECG
patterns in which urgent coronary angiography and revascularization may improve patient out-
comes.

INTRODUCTION also suggestive of adverse outcome and may

benefit from rapid transfer for coronary angiog-
Chest pain or other symptoms concerning for raphy. This article reviews specific high-risk ECG
acute coronary syndrome (ACS) continues to patterns that may represent acute myocardial
remain a major reason for presentation to the infarction (AMI) or identify impending AMI
emergency department. However, there is signifi- that benefits from early diagnostic coronary
cant heterogeneity in the spectrum of risk severity angiography.
of these patients, ranging from patients presenting
either with cardiac arrest or cardiogenic shock to
WELLENS SYNDROME
those patients presenting with benign noncardiac
chest pain. The electrocardiogram (ECG) remains This syndrome is a characteristic pattern present
a critically valuable tool in the physician’s arsenal in the precordial leads of the ECG in patients pre-
to diagnose patients and help with risk stratifica- senting with ACS that signifies the presence of a
tion. Although the management of ST-segment critical stenosis of the proximal left anterior
elevation myocardial infarction (STEMI) is straight- descending (LAD) coronary artery. Wellens T
forward and requires rapid reperfusion, there are waves were first described in 1982 from a series
multiple other high-risk ECG findings that are of 26 of 145 patients presenting with unstable
cardiology.theclinics.com

Disclosure Statement: The authors have nothing to disclose.

a
MedStar Heart and Vascular Institute, MedStar Washington Hospital Center, 110 Irving Street, NW, Washing-
ton, DC 20010, USA; b Department of Emergency Medicine, University of Maryland School of Medicine, 110
South Paca Street, Baltimore, MD 21201, USA; c Department of Emergency Medicine, University of Virginia
School of Medicine, PO Box 800699, 1215 Lee Street, Charlottesville, VA 22908, USA
* Corresponding author. Department of Emergency Medicine, University of Virginia School of Medicine, PO
Box 800699, 1215 Lee Street, Charlottesville, VA 22908.
E-mail address: [email protected]

Cardiol Clin 36 (2018) 13–26

http://dx.doi.org/10.1016/j.ccl.2017.08.002
0733-8651/18/Ó 2017 Elsevier Inc. All rights reserved.
14 Lipinski et al

angina who had initial negative cardiac enzymes. that develop AMI and death. A subsequent pro-
Wellens T waves are characterized by biphasic spective study in 1260 patients with unstable
T-wave inversions in leads V2 or V3 with an initial angina by the same group demonstrated that
positive deflection and subsequent terminal nega- 180 of the patients (14%) presented with Wellens
tive deflection (type A, w25% of patients) or sym- T waves, all of whom were shown to have greater
metric, often deep (>2 mm), T-wave inversions in than or equal to 50% stenosis of the LAD on coro-
the anterior precordial leads (type B, w75% of pa- nary angiography.3
tients).1 Although these changes are present in V2 Clinical management of patients with Wellens
and V3, they are found across the precordial leads, syndrome requires rapid recognition because it
commonly involving V4 but much less frequently signifies a large impending anterior AMI. Although
seen in V1.2 These characteristic changes typically medical therapy for ACS is obviously required,
develop after the resolution of chest pain. Howev- rapid transfer for urgent coronary angiography
er, patients may develop either ST-segment eleva- and possible revascularization is imperative.
tion or normalization of the ST segment and T Patients treated conservatively with medical ther-
wave with recurrence of chest pain.2 An example apy but without revascularization progress to
of Wellens T waves progressing to anterior STEMI AMI and potentially death.1 Therefore, although
is found in Fig. 1. Wellens syndrome also requires Wellens syndrome is not considered a STEMI
that there be absence of electrocardiographic equivalent, it is our clinical practice to take these
criteria for myocardial infarction, such as patho- patients urgently or emergent to the cardiac
logic Q waves or absence of R waves, because catheterization laboratory to avoid the develop-
the T-wave morphology seen with Wellens ment of anterior STEMI and associated pathologic
syndrome mimics the T-wave inversion pattern consequences.
found following a recent anteroseptal myocardial The clinical context of patients presenting with
infarction. Wellens syndrome is critical because there are a
The presence of Wellens syndrome carries sig- variety of ECG patterns that mimic Wellens syn-
nificant diagnostic and prognostic value. In the drome. It is essential because “pseudo-Wellens
initial series, the value of Wellens T waves was T waves” can also occur in a variety of clinic con-
not recognized until most developed anterior ditions. In the case of cocaine and intracranial
AMI. Of the 13 patients that underwent coronary hemorrhage, the cause of the pseudo-Wellens T
angiography in this initial group, 12 were found to waves may be the result of coronary spasm
have greater than or equal to 90% stenosis of involving the proximal LAD. Among patients with
the proximal LAD.1 Because the characteristic intracranial hemorrhage, the ECG can frequently
T-wave changes are a harbinger of a critical steno- demonstrate inverted T waves and QT prolonga-
sis in the proximal LAD, the prognostic importance tion.4–6 Patients with deep inverted T waves
was highlighted by the high percentage of patients have also been shown to have a characteristic

Fig. 1. Wellens syndrome converting to anterior STEMI. A 73-year-old woman with hypertension and hyperlipid-
emia presented to the emergency department with 2 hours of intermittent chest pain. (A) Her initial ECG demon-
strated Wellens syndrome (type II) with T-wave inversions in leads V2 and V3. (B) Repeat ECG was performed after
return of chest pain and demonstrated anterior STEMI. She underwent emergent coronary angiography, which
demonstrated a subtotal occlusion of the proximal LAD (99% stenosis).
 Evolving ECG Reperfusion Indications 15

apical hypertrophic cardiomyopathy variant.7 The ECG consistent with Wellens syndrome. For
following is a list of clinical presentations that example, as seen in Fig. 2, patients with chest
can present with an ECG with T-wave inversion pain and ECG suggestive of Wellens syndrome
or biphasic T waves in V2 or V3 that can mimic should be treated as an ACS, including emergent
Wellens syndrome: coronary angiography. For patients in whom the
diagnosis remains unclear, echocardiography
 Intracranial hemorrhage or stroke may be helpful because patients with Wellens syn-
 Hypertrophic cardiomyopathy drome often have anterior wall hypokinesis. Ulti-
 Coronary spasm in the case of cocaine use mately, appropriate diagnosis relies on careful
 Persistent juvenile T wave pattern assessment of both the ECG and obtaining an
 Pulmonary embolism accurate and comprehensive history.
 Digitalis effect
 Brugada syndrome
 Right bundle branch block POSTERIOR ACUTE MYOCARDIAL
INFARCTION
As this list shows, numerous clinical conditions
are associated with T-wave inversions or biphasic Myocardial injury pattern of the posterior wall,
T waves in the anterior precordial leads. Thus, clin- more correctly known as the inferolateral wall,
ical management should be tailored to the clinical can prove to be diagnostically challenging. Unlike
scenario. For example, patients with obtundation other myocardial regions that tend to produce a
and anterior precordial T-wave inversions on distinct ST-segment elevation pattern with recip-
ECG should be evaluated for neurologic injury rocal changes (anterior, inferior, and lateral), injury
rather than assuming the presentation is consis- pattern in the posterior wall results in the develop-
tent with ACS. The true clinical challenge occurs ment of a characteristic ST-segment depression in
in patients presenting with chest pain and an leads V1 to V3. The classic teaching with a

Fig. 2. Pseudo-Wellens T waves in apical hypertrophic cardiomyopathy. A 68-year-old woman with diabetes mel-
litus and poorly controlled hypertension presented to the emergency department with chest pain that developed
following 20 minutes of palpitations. (A) Her ECG demonstrated anterior T-wave inversions concerning for Well-
ens syndrome. She underwent urgent coronary angiography, which demonstrated nonocclusive coronary artery
disease. A left ventriculogram was performed, which demonstrated near complete obliteration of the left ventric-
ular cavity during systole. A cardiac MRI, with representative images in diastole (B) and systole (C), confirmed the
diagnosis of apical-variant hypertrophic cardiomyopathy.
16 Lipinski et al

posterior STEMI is that the diagnosis is made by artery may be electrocardiographically silent or
holding the ECG inverted horizontally and looking occur with subtle nonspecific ST or T-wave abnor-
through the back of the upside-down ECG. This malities, it is important to strongly consider the
leads the ST-segment depression seen in V1 clinical context when deciding whether or not to
through V3 to appear as contiguous ST-segment refer for emergent coronary angiography.
elevation. Posterior AMI may also be associated Fortunately, posterior STEMI often accom-
with a tall R wave in V1 or V2 (the mirror image of panies either inferior STEMI, lateral STEMI, or
a Q wave), prominent upright T waves in V1 to V3 both. A classic example of a posterolateral STEMI
(the mirror image of deeply inverted T waves), or caused by acute occlusion of the left circumflex
a combination of horizontal ST depression with artery is found in Fig. 3. Marked isolated ST
an upright T wave. Fortunately, a true isolated pos- depression and tall R waves in the right precordial
terior AMI occurs in only 3% to 11% of all STEMIs. leads (V1 to V3) in a clinical scenario consistent
In these cases, there may be no accompanying ST with STEMI is usually posterior STEMI. In addition
elevation on the ECG and the addition of posterior to adding posterior leads, repeating the ECG
leads to the standard 12-lead ECG may improve within 30 minutes looking for dynamic changes
diagnostic accuracy. Posterior leads should be and echocardiography looking for posterior wall
placed at the following locations8: V7, posterior motion abnormality may help in the identification
axillary line; V8, inferior angle of the scapula; and of a posterior AMI.
V9, left lateral edge of the spine.
As is standard, two contiguous leads with ST- LEFT BUNDLE BRANCH BLOCK
segment elevation of 1 mm in V7 to V9 or charac-
teristic horizontal ST-segment depression in leads Left bundle branch block (LBBB) results from fail-
V1 to V3 should enable a diagnosis of posterior ure to conduct a supraventricular rhythm through
STEMI. There is poor correlation between the R the left bundle branch of the Purkinje system.
wave in the anterior leads and the Q wave in pos- This leads the initial conduction to travel rapidly
terior leads, because only 50% of patients with through the right bundle branch with right ventric-
posterior AMI have both a tall R wave in V1 or V2 ular activation and subsequent activation of the
and Q waves in the posterior leads.9 However, left ventricle after transseptal activation. The
horizontal ST-segment depression in V1 to V3 ECG is characterized by a QRS duration greater
and ST-segment elevation in the posterior leads than 120 milliseconds with a predominantly nega-
have a greater correlation, with 85% of patients tive QS or rS in lead V1, whereas there is a broad,
with posterior AMI having both ST depression in notched monophasic R wave in lead V6. Leads I
V1 to V3 and ST elevation in the posterior leads.9 and aVL are associated with ST depression and
Although ST-segment depression in V1 to V3 is often T-wave inversion, which is in keeping with
present in 61% to 92% of posterior AMI, ST- the concept of appropriate discordance, wherein
segment elevation in the posterior leads is an the ST segment or T-wave complex is in the oppo-
excellent marker of posterior AMI and occurs in site direction from the primary terminal portion of
91% to 100% of posterior AMI.9,10 However, the QRS complex. For instance, because of the
because acute occlusion of the left circumflex monophasic R wave in lead V6, there is usually

Fig. 3. Posterolateral STEMI. A 56-year-old man presented to the emergency department with sudden-onset
crushing chest pain. ECG demonstrated posterolateral STEMI with deep ST-segment depression in leads V1 to
V3 and aVR along with ST-segment elevation in leads I, II, aVL, and V4 to V6. Emergent coronary angiography
demonstrated a total occlusion of a dominant left circumflex artery.
 Evolving ECG Reperfusion Indications 17

negative ST segment deflection that slurs into a changes is straightforward and requires transfer of
deep T-wave inversion. the patient for emergent coronary angiography.
LBBB can be a sign of underlying heart disease However, the challenge lies with atypical symp-
and is frequently associated with myocardial toms, such as atypical chest pain or shortness of
fibrosis. It is also important to note that pacing of breath that may represent an anginal equivalent.
the right ventricle results in LBBB morphology on Interventional cardiologists frequently hesitate to
ECG and has a nearly identical activation take patients to the cardiac catheterization labora-
pattern.11 However, identification of acute tory with LBBB of indeterminate age. However,
ischemia in the setting of pre-existing LBBB is this resistance to perform angiography given un-
challenging but is often associated with exaggera- certainty whether the LBBB is truly new may delay
tion of discordant ST-segment depression or appropriate revascularization and increase risk to
concordant ST-segment deviation. The clinical the patient. Indeed, a recent meta-analysis of
presentation of patients with AMI and LBBB takes 105,861 patients presenting with AMI from eight
the following forms: new LBBB as a STEMI equiv- studies demonstrated that patients presenting
alent; new ischemic changes with pre-existing with LBBB actually have increased risk of 30-day
LBBB; and chest pain in setting of LBBB of inde- and 1-year mortality along with increased risk of
terminate age, which may reflect chronic ischemic developing recurrent heart failure.12 However, it
heart disease or underlying cardiomyopathy. remains unclear whether delay in therapy has
In addition to careful evaluation of the ECG and any impact on outcomes or whether these patients
comparison with previous ECGs, if available, the simply have a worse outcome because of their
clinical presentation is critical in determining older age and greater comorbidities.
whether emergent coronary angiography is neces- Since its publication in 1996, the Sgarbossa
sary. An example of the value of prior ECGs and criteria13 have been used to identify the presence
careful history taking is found in Fig. 4. Typical of acute ischemia in a patient who presents with
chest pain and a new LBBB or LBBB with ischemic chest pain and LBBB. The Sgarbossa criteria use

Fig. 4. LBBB in the setting of cocaine abuse. A 64-year-old man with unclear cardiac history presented to the
emergency department with chest pain and palpitations following cocaine use. (A) His initial ECG demonstrated
sinus tachycardia with heart rate of 130 bpm with an LBBB and diffuse discordant ST deviations greater than
5 mm in the anterior precordial leads. His chest pain resolved with nitroglycerin and lorazepam. A bedside echo-
cardiogram demonstrated a left ventricular ejection fraction of 30% with anterior wall akinesis and severe ante-
roapical thinning consistent with prior anterior myocardial infarction. (B) A prior ECG was obtained, which
demonstrated the LBBB was old and previously had similar morphology, with more pronounced ST deviation
likely secondary to tachycardia. On further questioning, the patient described a prior myocardial infarction
without intervention. His cardiac biomarkers were negative and he was ultimately discharged from the emer-
gency department.
18 Lipinski et al

a point-based system to determine the likelihood not exclude the presence of AMI.17 To improve
of an ACS with an underlying LBBB. There are the diagnostic accuracy of the Sgarbossa criteria,
three key components of the Sgarbossa criteria: Smith and colleagues18 demonstrated a signifi-
(1) concordant ST-segment elevation greater cant improvement in diagnostic accuracy for
than 1 mm, which is strongly suggestive of AMI identification of STEMI in the setting of LBBB by
(odds ratio, 25); (2) concordant ST-segment replacing the third component of the Sgarbossa
depression greater than 1 mm in leads V1 to V3, criteria (>5 mm of ST-segment elevation discor-
which is also strongly suggestive of AMI (odds ra- dant from the QRS complex) with the ratio of
tio, 6); and (3) ST-segment elevation greater the ST-segment deviation adjusted for the S
than 5 mm discordant from QRS complex, which wave by improving sensitivity and only slightly
is only somewhat suggestive of AMI (odds ratio, reducing specificity. Echocardiography may also
4). It is important to remember that although the help with risk stratification. Despite the character-
Sgarbossa criteria are specific (96%), they have istic abnormal septal wall motion or “septal
a low sensitivity (36%).13 bounce” on echocardiography in patients with
In a subsequent series of patients with LBBB LBBB, echocardiography may also help predict
presenting with presumed AMI, patients with a which patients actually have ACS among patients
higher Sgarbossa score were found to have a presenting to the emergency department with
higher mortality than those with a score less LBBB and chest pain.19
than 3 (23.5% vs 7.7% at 30 days, respectively; In the 2013 American Heart Association/Amer-
P<.001).14 To further evaluate the utility of the ican College of Cardiology Foundation Guidelines
Sgarbossa Criteria, a retrospective analysis for the Management of STEMI, new or “presumed
from the Mayo Clinic’s STEMI network demon- new” LBBB as a STEMI equivalent is addressed.20
strated that only 14 of 36 patients presenting A new LBBB as a STEMI equivalent occurs infre-
with “new or presumably new” were ultimately quently21 and “should not be considered diag-
diagnosed with ACS.15 Another study of 102 pa- nostic of AMI in isolation.” However, it is
tients with chest pain and LBBB suggested that important to remember that ischemic injury of the
concordant ST-segment changes are the great- conduction system leading to the development
est predictor for true STEMI and play the largest of an LBBB results from a proximal LAD occlusion
factor in determining which patients require above the level of the first septal perforator artery
emergent coronary angiography.16 This seems and typically is dramatic. As demonstrated in
consistent with a meta-analysis on the topic that Fig. 5, these patients often have dramatic clinical
demonstrated that greater than or equal to presentations and ECGs. Thus, the decision to
1 mm of concordant ST elevation or greater take a patient emergently for cardiac catheteriza-
than or equal to 1 mm ST depression in leads V1 tion requires a compatible clinical scenario, in
to V3 was effective in diagnosing AMI in patients addition to the presence of new LBBB or old
with LBBB, whereas a Sgarbossa score of 0 did LBBB with ischemic changes.

Fig. 5. LBBB with anterior STEMI. An 80-year-old woman with past medical history of diabetes mellitus type II,
hypertension, hyperlipidemia, and previously normal ECG presented via ambulance to the emergency depart-
ment with profound shortness of breath and chest pressure. Her ECG demonstrated sinus tachycardia with a heart
rate of 120 bpm along with discordant ST-segment deviation (>5 mm) in V2 and V3 and concordant ST-segment
elevation in V4 to V5 (>1 mm) consistent with new LBBB and anterior STEMI. She was intubated because of acute
hypoxic respiratory failure from pulmonary edema and underwent emergent coronary angiography with primary
percutaneous coronary intervention with stenting of the proximal LAD above the level of the first septal perfo-
rator. Her left ventricular ejection fraction was 20% and she required intra-aortic balloon pump for cardiogenic
shock.
 Evolving ECG Reperfusion Indications 19

PACED RHYTHM usually paced by their device? Interrogation of

the device is critical to determine how often
The presence of a cardiac pacemaker or the patient is paced by their device and
implantable cardiac defibrillator (ICD) may whether the patient required tachytherapies,
complicate the interpretation of the ECG in pa- such as shocks or antitachycardial pacing.
tients who present to the emergency department
with chest pain. Not only may the interpretation The previously listed information may be critical
of the ECG be challenging, but there is vital in- in determining the severity of a patient’s illness.
formation in the clinical history that may not be For example, a patient that rarely requires ventric-
intuitive for noncardiologists, which may help ular pacing who now presents with chest pain and
clarify the clinical scenario. Next is a list of infor- a ventricular paced rhythm is concerning and im-
mation that should be identified for all patients plies either new ischemia-mediated heart block
presenting with chest pain who have a cardiac or profound bradycardia. Patients with right ven-
device: tricular pacing not only have an ECG pattern
consistent with LBBB but also have a similar elec-
1. Does the patient have an ICD or only a perma- tromechanical activation pattern of the ventri-
nent pacemaker? It is important to recognize cles.11 Thus, interpretation of the ECG in patients
that all ICDs have the ability to pace the with an underlying ventricular paced rhythm is
ventricle. challenging in the setting of chest pain. However,
2. Which company is the device manufacturer? a patient with an atrial-paced, ventricular-sensed
(Medtronic, Boston Scientific/Guidant, St Jude’s/ rhythm should have little change to their underly-
Abbott, or Biotronik) ing ECG because ventricular depolarization and
3. Is there a single right ventricular lead, dual- repolarization are unaffected. The obvious ques-
chamber device (right atrial and right ventricular tion is whether the Sgarbossa criteria can be
lead), or biventricular device (right ventricular applied in the setting of a paced rhythm to identify
lead, left ventricular lead, right atrial lead)? If patients with ongoing myocardial ischemia or
the patient does not know this information, injury. A meta-analysis of three studies suggested
the chest radiograph is not only able to identify that the Sgarbossa criteria may be helpful in iden-
how many leads and whether the device is an tifying AMI in patients with a ventricular paced
ICD, but may also help identify the device rhythm.22 An example of ST-segment depression
manufacturer. in leads V1 through V3 in a patient with a ventricular
4. What was the clinical indication for device paced rhythm is found in Fig. 6 and correctly iden-
placement? (eg, syncope, complete heart tified the presence of an inferoposterior STEMI.
block, cardiomyopathy)
5. When was the device last interrogated?
DE WINTER ELECTROCARDIOGRAPHIC
6. If an ICD, has the patient ever been shocked? If PRESENTATION
yes, when was the patient last shocked?
7. For patients with ventricular pacing, it may be The de Winter ECG presentation includes upslop-
helpful to ask the patient whether they are ing ST-segment depression in leads V1 to V4,

Fig. 6. Paced inferoposterior STEMI. ECG obtained following ventricular fibrillation cardiac arrest in patient with
chest pain. ECG demonstrates an AV paced rhythm with evidence of ST-segment depression in leads V2 to V4
consistent with concordant ST-segment depression (>1 mm) and discordant ST deviation that might otherwise
be missed in leads II, III, and aVF. A rapid bedside echocardiogram confirmed inferolateral wall hypokinesis
and left ventricular ejection fraction of 35%. Emergent coronary angiography demonstrated an occluded prox-
imal dominant left circumflex artery.
20 Lipinski et al

prominent T waves in the same anterior distribu- recorded on average 1.5 hours after symptom
tion, and ST-segment elevation in lead aVR onset and persisted (ie, static without appreciable
(Fig. 7). This constellation of ECG findings is asso- evolution) until the obstruction was definitively
ciated with proximal LAD occlusion and significant managed via percutaneous coronary intervention.
risk for anterior wall STEMI, if not a STEMI- This presentation was associated with significant
equivalent pattern. Patients presenting with this myocardial injury.23 One year later, Verouden and
ECG pattern are frequently ill in appearance and colleagues25 reported this same ECG pattern in
rapidly progress to STEMI. 35 patients (2%) out of 1890 individuals undergo-
The electrophysiologic cause of this pattern re- ing percutaneous coronary intervention for LAD ar-
mains uncertain. It has been theorized that intra- tery obstruction. This ECG pattern (see Fig. 7 A, B)
ventricular conduction delay resulting from consisted of the following ECG features:
anatomic variations of the Purkinje fiber system  Upsloping ST-segment depression greater
is a possible explanation for the observed ECG than 1 mm at the J point in the precordial
pattern.23 Potential support for this theory is found leads
in the observation that ligation of the LAD artery  Continuation of the ST-segment depression
does not produce ST-segment elevation in mice into tall, prominent, symmetric T waves in
homozygous for a particular cardiac channel the precordial leads
(the K-ATP channel), which changes intraventric-  ST-segment elevation (0.5–2 mm) in lead aVR
ular conduction24; thus, acute coronary ischemia  The absence of other, anatomically oriented
potentially alters activation of these KATP chan- ST-segment elevation
nels, contributing to the J-point depression with
prominent T waves in the anterior leads.23 Compared with patients with traditional STEMI
In 2008, de Winter and colleagues23 published a presentations, these patients tended to be male,
series of 30 patients, describing a newly noted younger in age, and hypercholesterolemic.25
ECG pattern associated with acute LAD artery oc- Most recently, de Winter and coworkers26 again
clusion. Among 1532 patients with acute anterior reported this pattern, emphasizing its unique
wall myocardial infarction, these 30 individuals appearance, association with proximal LAD artery
(2%) were found to have proximal LAD artery oc- obstruction, and the need for prompt recognition
clusion at cardiac catheterization. The ECGs and urgent coronary reperfusion.
demonstrated a characteristic, unique pattern, Goebel and colleagues27 noted an important dif-
including 1- to 3-mm upsloping ST-segment ference in the de Winter presentation, compared
depression at the J point in leads V1 to V5; this with prior reports.23,25 Previous reports of the de
unusual-appearing ST-segment depression Winter ECG presentation noted its static appear-
continued tall, prominent, symmetric T waves. ance (ie, lack of evolution to STEMI), in essence
In addition, lead aVR frequently revealed 1- to describing a STEMI equivalent pattern. Goebel
2-mm ST-segment elevation; interestingly, and colleagues27 reported an adult male patient
anatomically associated ST-segment elevation with chest pain and the de Winter ECG pattern;
was lacking in all cases.23 The ECG pattern was over a 2-hour period, the patient progressed

Fig. 7. de Winter Pattern. Pronounced ST segment depression with J pont depression continuing into a promi-
nent T wave in leads V2 to V4. In addition, note the ST segment elevation in lead aVR and widespread ST segment
depression in numerous other leads. (From Macias M, Peachey J, Mattu A, et al. The electrocardiogramin the ACS
patient: high-risk electrocardiographic presentations lacking anatomically oriented ST-segment elevation. Am J
Emerg Med 2016;34(3):611–7; with permission.)
 Evolving ECG Reperfusion Indications 21

from the precordial J-point depression with prom- associated with severe LMCA disease defined as
inent T wave to obvious anterior ST-segment a greater than or equal to 50% stenosis.29 Howev-
elevation, consistent with STEMI. Cardiac cathe- er, ST elevation in aVR has a poor specificity for
terization demonstrated a mid-LAD artery significant LMCA disease. The following is a list
occlusion. of conditions associated with ST-segment eleva-
Whether the de Winter ECG presentation repre- tion in lead aVR:
sents either a STEMI equivalent pattern or a high-
risk electrocardiographic presentation with rapid  Left main coronary artery disease
progression to STEMI, it is known that significant  Thoracic aortic dissection, potentially involving
LAD artery occlusion is usually responsible for the coronary arteries or coronary cusps
this clinical entity. Although much is not known  Massive pulmonary embolism
about the de Winter ECG pattern, this electrocar-  Global ischemia, as seen with hemorrhagic
diographic presentation in a patient suspected of shock or rapid arrhythmias
ACS should prompt a rapid response with consid-  Left ventricular hypertrophy
eration of urgent coronary angiography and appro-  LBBB
priate intervention.  Coronary vasospasm, consider cocaine
abuse
 Profound metabolic or electrolyte abnormal-
ELEVATION IN LEAD aVR ity, often seen following cardiac arrest
 Myocarditis or pericarditis
Despite not having a clear role in identification of
STEMI, the presence of ST-segment elevation in In the setting of pulmonary embolism, the pres-
lead aVR has received increased attention ence of ST-segment elevation in lead aVR also
because of its value in identifying critically ill correlates with increased cardiac biomarkers,30
patients. In patients with out-of-hospital cardiac implying not only a larger pulmonary embolism
arrest, the presence of ST-segment elevation in but also greater risk for adverse outcomes.
aVR was an independent predictor of coronary Indeed, ST-segment elevation in lead aVR, espe-
artery occlusion and may help identify which pa- cially if accompanied by elevation in the anterior
tients with cardiac arrest benefit from emergent leads, in the setting of pulmonary embolism may
coronary angiography despite not having a classic portend an ominous outcome.31 Further discus-
STEMI on ECG.28 An example of ST-segment sion of LMCA follows.
elevation in aVR with widespread ST-segment
depression following cardiac arrest is found in WIDESPREAD ST-SEGMENT DEPRESSION
Fig. 8. The constellation of widespread ST-
segment depression with ST-segment elevation LMCA occlusion is suggested by other ECG pat-
in lead aVR is extremely concerning for severe terns beyond anterior wall STEMI with or without
left main coronary artery (LMCA) disease or ST-segment elevation in lead aVR. In fact, a large
three-vessel coronary artery disease. In a retro- number of patients with LMCA occlusion may
spective study of patients with cardiogenic shock present with typical STEMI patterns.17 It is
and AMI, the presence of ST-segment elevation important to recognize lesser known ECG pat-
in lead aVR was the only variable independently terns indicating the LMCA as the culprit artery.19

Fig. 8. Diffuse ST-segment depression with ST elevation in aVR. A patient presented following PEA cardiac arrest.
ECG demonstrates widespread ST-segment depression (I, II, avF, V3 to V6) with ST-segment elevation in lead aVR.
Because of concern for left main coronary artery disease, the patient underwent emergent coronary angiog-
raphy, which demonstrated normal coronary arteries. Urine drug screen was positive for cocaine suggesting cor-
onary spasm as the cause. PEA, pulseless electrical activity.
22 Lipinski et al

One such ECG manifestation of LMCA occlusion occlusion. They reviewed the ECG of 113 consec-
is diffuse ST-segment depression (Fig. 9 A, B). utive patients with symptomatic ACS and
Widespread ST-segment depression, at times compared the electrocardiographic findings with
without coexisting ST-segment elevation, can the coronary anatomy determined at cardiac cath-
also indicate occlusion of the LMCA; this pattern eterization. They reported that ST-segment
may not be identified in timely fashion, thus depression in leads I, II, and V4 to V6 was seen
delaying intervention. The addition of ST- frequently in patients with LMCA stenosis; if lead
segment elevation in lead aVR to widespread aVR ST-segment elevation was also noted, this
ST-segment depression increases the likelihood combination pattern identified 90% of patients
of LMCA occlusion. with clinically significant LMCA occlusion. The
Two cautionary comments must be made with sensitivity for significant LMCA when both wide-
respect to the term LMCA occlusion. First, com- spread ST-segment depression and lead aVR
plete occlusion of the LMCA rapidly leads to ante- ST-segment elevation were present was 90%.
rior STEMI, cardiogenic shock, and cardiac arrest. Another objective manifestation of widespread
Thus, the term incomplete left main coronary oc- ST-segment depression indicative of LMCA occlu-
clusion is a more accurate term to describe these sion was a total summation of ST-segment devia-
high-risk ACS presentations. Second, these pat- tion being greater than 12 mm across the 12-lead
terns can also be seen in other high-risk ECG pre- ECG. Kosuge and colleagues33 expanded on this
sentations, including proximal LAD occlusion, early work with an investigation of 310 patients
severe triple-vessel coronary artery occlusive dis- admitted to the coronary care unit with an initial
ease, and diffuse subendocardial ischemia diagnosis of non–ST-segment elevation ACS.
following periods of significant hemodynamic They found similar results, noting that widespread
compromise. Although these various other pre- ST-segment depression and ST-segment eleva-
sentations are high-risk, the management ap- tion in lead aVR was associated frequently with
proaches are likely different compared with LMCA occlusion. In fact, they noted that diffuse
LMCA occlusion scenarios. ST-segment depression greater than 1.0 mm
Gorgels and colleagues32 identified widespread was present in more than 80% of patients with
ST-segment depression as an indicator of LMCA significant LMCA stenosis.

Fig. 9. Left main coronary artery occlusion. (A) Widespread ST-segment depression (leads I, II, aVL, and V2 to V6)
along with ST-segment elevation in lead aVR. (B) Widespread ST-segment depression (leads I, II, aVL, and V2 to V6)
along with ST-segment elevation in lead aVR. (ECG image Courtesy Dr Scott McCann.)
 Evolving ECG Reperfusion Indications 23

Fig. 10. Nonanatomic ST-segment elevation resulting from D1 artery lesion producing acute myocardial infarc-
tion. Note the ST-segment elevation in leads aVL and V2. In addition, note the ST-segment depression in leads
II, III, aVF, and V3 to V6.

The value of widespread ST-segment depres- leads (II, III, and aVF) and an anterior STEMI ex-
sion alone was compared with the coexistence hibits ST-segment elevation in at least two leads
of widespread ST-segment depression and lead from V1 to V4.
aVR ST-segment elevation. Taglieri and col- The LAD artery is the most commonly identified
leagues34 considered this issue in patients with coronary occlusion resulting in myocardial infarc-
ECGs showing widespread ST-segment depres- tion.35 An evolving area of ACS study has demon-
sion with and without STE in lead aVR and the strated a correlation between characteristic ECG
association with LMCA occlusive disease. The in- changes and occlusion of branches arising from
vestigators noted that widespread ST-segment this artery that do not meet the classic definition
depression greater than 0.5 mm when occurring of AMI with ST-segment elevation in two anatom-
with ST-segment elevation in lead aVR greater ically contiguous leads. An example of the nonan-
than 0.1 mm was present in a significantly larger atomic distribution of ST-segment elevation and
proportion (P<.001) of patients with significant its relation to significant ACS, including STEMI,
LMCA occlusion when compared with those indi- can occur with occlusion of the first diagonal
viduals with widespread ST-segment depression branch of the LAD artery. This artery provides
by itself. Although the combination of diffuse perfusion to the anterolateral wall of the left
ST-segment depression and lead aVR ST- ventricle as it courses over these two segments.35
segment elevation was more predictive of LMCA From the perspective of the 12-lead ECG, occlu-
occlusion, the presence of diffuse ST-segment sion of the first diagonal branch of the LAD (D1)
depression was also associated with this high- artery can present with ST-segment elevation in
risk coronary pattern. LMCA disease represents leads aVL and V2, along with ST-segment depres-
one of the highest risk disease states encoun- sion in the inferior leads and, at times, the lateral
tered in the cardiac catheterization laboratory leads (Fig. 10). Occlusion of the D1 artery places
and its rapid detection in the emergency depart- a large portion of the left ventricle in ischemic jeop-
ment may play a critical role in stabilization of ardy and thus must be recognized early with the
these patients. application of intervention in timely fashion.
Sclarovsky and colleagues36 identified “.a
NONANATOMIC ST-SEGMENT ELEVATION special electrocardiographic subtype of acute
myocardial infarction” manifested by “.ST-
“Nonanatomic” used in this section refers to the segment elevation in non-consecutive leads.” In
lack of traditionally taught anatomic regional ST- a series of eight patients with AMI resulting from
segment elevation and its association with STEMI D1 artery occlusion, these investigators described
infarct patterns. Current guidelines recommend the ECG findings, including ST-segment elevation
that electrocardiographic criteria for STEMI diag- greater than 1 mm in leads aVL and V2; ST-
nosis requires at least two anatomically contig- segment depression in leads III, aVF, V4, and V5;
uous ECG leads demonstrating ST-segment and variable ST-segment elevation in lead I.
elevation in a single coronary anatomic distribu- Birnbaum and colleagues37 considered AMI pa-
tion. For example, an inferior STEMI demonstrates tients with ST-segment elevation in lead aVL. In a
ST-segment elevation in at least two of the inferior study group of 57 patients with lead aVL elevation,
24 Lipinski et al

eight individuals demonstrated ST-segment eleva- stenosis high in left anterior descending coronary
tion additionally in lead V2. These patients had the artery in patients admitted because of impending
D1 artery unequivocally identified at cardiac cath- myocardial infarction. Am Heart J 1982;103(4 Pt 2):
eterization as the culprit vessel. The investigators 730–6.
concluded that ST-segment elevation in leads 2. Rhinehardt J, Brady WJ, Perron AD, et al. Electrocar-
aVL and V2 was associated with 89% positive pre- diographic manifestations of Wellens’ syndrome. Am
dictive value for anterior or anterolateral resulting J Emerg Med 2002;20(7):638–43.
from a D1 arterial occlusion. Similar results have 3. de Zwaan C, Bar FW, Janssen JH, et al. Angio-
been reported by other investigators.38 graphic and clinical characteristics of patients with
A nonanatomic distribution of ST-segment unstable angina showing an ECG pattern indicating
elevation in leads aVL and V2 can be the sole critical narrowing of the proximal LAD coronary
electrocardiographic abnormalities encountered artery. Am Heart J 1989;117(3):657–65.
in such a high-risk ACS presentation. It must 4. van Bree MD, Roos YB, van der Bilt IA, et al. Preva-
be stressed that this ECG presentation does lence and characterization of ECG abnormalities af-
not include two anatomically contiguous leads ter intracerebral hemorrhage. Neurocrit Care 2010;
with ST-segment elevation; rather, single leads 12(1):50–5.
with ST-segment elevation are seen in two non- 5. Stober T, Kunze K. Electrocardiographic alterations
anatomically (classically, nonanatomic) distribu- in subarachnoid haemorrhage. Correlation between
tions. This type of ACS presentation can spasm of the arteries of the left side on the brain and
involve large amounts of myocardium in jeop- T inversion and QT prolongation. J Neurol 1982;
ardy; it must be recognized and managed 227(2):99–113.
appropriately, despite its nontraditional ECG 6. Yamour BJ, Sridharan MR, Rice JF, et al. Electrocar-
presentation. diographic changes in cerebrovascular hemor-
rhage. Am Heart J 1980;99(3):294–300.
7. Suzuki J, Watanabe F, Takenaka K, et al. New sub-
SUMMARY
type of apical hypertrophic cardiomyopathy identi-
The ECG continues to play a critical role in deter- fied with nuclear magnetic resonance imaging as
mining which patients require urgent coronary an underlying cause of markedly inverted T waves.
angiography and revascularization. It is therefore J Am Coll Cardiol 1993;22(4):1175–81.
important to not only be familiar with the obvious 8. Lindridge J. True posterior myocardial infarction: the
indications for emergent cardiac catheterization, importance of leads V7-V9. Emerg Med J 2009;
but also to be able to identify more subtle ECG 26(6):456–7.
patterns in which urgent coronary angiography 9. Agarwal JB, Khaw K, Aurignac F, et al. Importance
and revascularization may improve patient out- of posterior chest leads in patients with suspected
comes. Although the ability to recognize these myocardial infarction, but nondiagnostic, routine
ECG patterns may be helpful, clinical presentation 12-lead electrocardiogram. Am J Cardiol 1999;
and the patient’s symptomatology remains of 83(3):323–6.
paramount importance in determining which pa- 10. Matetzky S, Freimark D, Feinberg MS, et al.
tients require urgent coronary angiography or Acute myocardial infarction with isolated ST-
further stabilization in the cardiovascular intensive segment elevation in posterior chest leads V7-9:
care unit. Because acute coronary occlusion of the “hidden” ST-segment elevations revealing acute
left circumflex artery may be electrocardiographi- posterior infarction. J Am Coll Cardiol 1999;
cally silent, ongoing chest pain resistant to medical 34(3):748–53.
therapy must signal to the clinician need for 11. Vassallo JA, Cassidy DM, Miller JM, et al. Left ven-
continuing evaluation. It is through continued tricular endocardial activation during right ventricu-
practice at ECG interpretation, careful assessment lar pacing: effect of underlying heart disease.
of the patient’s symptoms, thorough physical J Am Coll Cardiol 1986;7(6):1228–33.
examination, and coordinated care from the emer- 12. Al Rajoub B, Noureddine S, El Chami S, et al. The
gency room physicians, cardiologist, and other prognostic value of a new left bundle branch block
care providers that optimal outcomes in patients in patients with acute myocardial infarction: a sys-
presenting with chest pain to the emergency tematic review and meta-analysis. Heart Lung
department can be achieved. 2017;46(2):85–91.
13. Sgarbossa EB, Pinski SL, Barbagelata A, et al. Elec-
trocardiographic diagnosis of evolving acute
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